Recent Breakthroughs in the Treatment of Alzheimer’s Disease

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This month, two new breakthroughs in Alzheimer’s disease research have been announced: the drug company Biogen has claimed to have manufactured the first treatment of its kind for the disease, having previously shelved the same project earlier this year. A few days later, neuroscientists at the University of Southampton announced they had discovered a key window of intervention in Alzheimer’s disease by researching how it develops and spreads in the brain. 

Alzheimer’s disease (AD), one of the primary causes of dementia, has become a major problem for the developed world since it was first discovered over 100 years ago. Ageing populations due to advances in healthcare and life expectancies in nations above the Brandt line are increasingly having to manage a large proportion of their over-75 citizenry suffering from a condition that has proven devastating, both financially and socially. AD is said to be ‘a disease of the brain’; the basic cells in the brain (neurons) are attacked by the disease and wither away over a long period of time. This manifests initially as the normal issues associated with ageing, such as short-term memory loss, impaired concentration and general disorientation. As the disease progresses, however, and as the neurons involved in cognition and memory are killed off in large numbers, a total loss of memory and language faculties follows, with physical and mental incapacitation ultimately impeding an individual’s ability to lead a normal and independent lifestyle. AD has come to be recognised as a major health problem in the UK and elsewhere in recent decades.

The exact mechanism that leads to people getting AD is still unclear, but the general consensus is that it involves a toxic buildup of abnormal proteins in the brain; beta-amyloid and tau. These come about through the ‘misfolding’, or faulty production of the protein structures, and as the amounts of these proteins accumulate and clump together in the neurons over time, this has a devastating effect on brain function.

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The U.S. drug company Biogen has just submitted a ‘groundbreaking’ new treatment called Aducanumab to federal authorities for regulatory approval. While not a cure, it is nonetheless the first therapy that can slow the progression of AD; a significant achievement given that current treatments can only give an early warning of disease risk or help ease the symptoms. This came as a great surprise to the scientific community, as the Aducanumab project was previously discontinued in March this year due to disappointing results at the trial stage, highlighting the long and arduous process involved in manufacturing new drugs.

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Aducanumab works by binding to beta-amyloid protein deposits in the brain and ‘sweeping’ them out. While this doesn’t prevent the creation of new toxic proteins, it stops them building up and thus slows progression of AD. This in turn slows the cognitive decline seen in AD sufferers, allowing them to preserve their memory and day-to-day living skills for longer. Biogen has stated that patients in their clinical studies on a high dose of Aducanumab had 23% less cognitive decline after 18 months than those on a placebo (dummy drug). It is these patients that Biogen will initially offer the treatment to if Aducanumab is approved and brought to the market. Biogen’s chief executive Michel Vounatsos said: “We are hopeful about the prospect of offering patients the first therapy to reduce the clinical decline of Alzheimer’s disease.

Hilary Evans from Alzheimer’s Research UK said:

People affected by Alzheimer’s have waited a long time for a life-changing new treatment and this exciting announcement offers new hope that one could be in sight. Taking another look at aducanumab is a positive step for all those who took part in the clinical trials and the worldwide dementia research community. As more data emerges, we hope it will spark global discussions about the next steps for delivering much-needed treatments into people’s hands.

Meanwhile, researchers at the Southampton Neuroscience Group (SoNG) in the Faculty of Environmental & Life Sciences have made a significant development in understanding how Alzheimer’s disease spreads through the brain by studying the buildup of other protein involved in AD; tau. As stated previously, the exact mechanisms behind this remain rather obscure, but by studying the effects of tau in mice brains the team discovered that there was an interval period where tau was building up but the neurons remained unaffected and functioned normally.

Research supervisor Dr. Katrin Deinhardt, a Neuroscience lecturer at UoS, said:

We saw that misfolding tau was not immediately toxic and that the affected cells could tolerate the build-up better than we anticipated. This is a really positive outcome and highlights that there is a window of time where therapeutic intervention could take place to rescue neurons with tau pathology.

Grace Hallinan, a PhD student at the University of Southampton when she carried out this study, added:

We were really excited to find that neurons with misfolded tau could remain healthy, because this suggests they could be saved before the occurrence of the cell death that leads to brain shrinkage and memory problems. We hope that our findings will encourage further research into this therapeutic window in order to slow or even stop the progression of Alzheimer’s disease

The results of the SoNG study were published in The Journal of Neuroscience, and the University of Southampton once again affirmed its status as an internationally-renowned Russell Group centre of research. Alzheimer’s Research UK has stated that they seek to build on this new information and fund further research into the targeting of the tau protein in AD treatment.

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These two discoveries have overcome significant hurdles in understanding the origins of AD. While a cure for dementia will no doubt be discovered eventually, for now a healthy lifestyle and mental well-being will go far in slowing down the disease and help people continue to live their lives to the fullest as they get older.

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Sub-editor 2019/20. Third Year Neuroscience student with a particular interest in concepts where innovation can translate science-fiction to science-reality

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